Sleep Apnea and Cardiovascular Diseases

Most of us spend between a quarter and a third of our lives sleeping, so any disorder that occurs during this period not only it affects our sleep and homeostasis but also the rest of the day. Snoring can often become annoying, especially for those who hear it, but most often, it can lead to cardiovascular problems or hide them, especially in combination with repeated episodes of apnea.

The condition, called sleep apnea (SAS) is a breathing disorder associated with sleep and characterized by repetitive episodes of reduced inspiratory flow due to upper airway obstruction during sleep. These episodes often wake up the person and prevent restful sleep. It is often associated with hypertension (HTA), arrhythmias, stroke or heart failure.

Although measurement techniques or the definition may vary, most studies have shown that about 1 in 5 adults has at least a mild form of SAS, and the number is growing due to the global increase of obesity. However, 85% of patients with significant clinical symptoms have not been diagnosed. Despite the high cost and low availability, polysomnography (PSG) remains the main recommendation of diagnosis, resulting in a discrepancy between the demand and the current capacity of diagnosing it in Romania.

When SAS was originally diagnosed and documented as an individual condition, patients were referred to as “type Pickwickian” which refers to middle-aged men with morbid obesity and constantly asleep. This stereotype has influenced the screening of patients with SAS, which is over-represented by these features. But today we know that SAS is rare in women or in normal-weight people and is more common in the elderly compared to the middle-aged.

Most people with vascular disease remain undiagnosed, largely because of the lack of awareness among physicians about this association. All hypertensive patients, who are obese or who have heart failure should be rotinely questioned about SAS, and in the case they are symptomatic, sleep study should be recommended. Using simple questions such as “Do you fall asleep often during the day?” “Does it happen to snore at night?” or “Are you tired in the morning when you wake up?”, the vast majority of patients with this pathology can be identified. There are, of course, standard methods such as the Epworth Sleepiness Scale, which uses a set of questions and provides a fast assessment of fatigue and there are also recently developed new applications for mobile platforms that simplify the diagnostic algorithm. (http://sasscore.appspot.com/)

Approximately half of the patients with SAS are hypertensive, and among the hypertensive patients, 30% of them have SAS, most often undiagnosed. Obstructive sleep apnea syndrome has been proposed as an independent risk factor in the development of essential hypertension because it may precede the onset. There are numerous mechanisms by which SAS affects the blood pressure and causes organ damage, such as negative intrathoracic pressure, nocturnal hypoxemia, hypercapnia, which result in increased oxidative stress on the body, induction of inflammatory responses and endothelial damage.

Cardiac failure

The direct mechanism hrough which SAS could induce left ventricular systolic dysfunction is by increasing the blood pressure and the higher it is during sleep, the grater the risk of developing ventricular hypertrophy. Treatment with CPAP (Continuous Positive Airway Pressure) can eliminate recurrent hypoxia and reduces nocturnal hypertension and the heart rate simultaneously. Several studies have shown an improvement in the ejection fraction and an even lower rate of mortality in patients receiving CPAP compared to those untreated, but randomized clinical trials are needed to assess this benefit.

Strokes

Obstructive sleep apnea syndrome significantly increases the risk of cerebrovascular accidents (CVA) or all-cause mortality, and this increase is independent of other risk factors such as hypertension. Patients with this pathology have a risk 2 times higher of developing a stroke, and this risk increases with the severity of SAS. According to recent studies, up to 60% of patients who have had a stroke have a high degree of sleep apnea; these patients do not show daytime fatigue as a symptom and screening is important for those with fragmented sleep, snoring or fatigue.

Repeated episodes of hypoxemia, sympathetic activation, and transmural pressure changes that occur in SAS are mechanisms that predispose to the occurrence of atrial fibrillation (AF). Although sleep apnea has been associated with left atrial enlargement, this leads to the assumption that the AF has not yet been demonstrated. In contrast, arrhythmias are rather related to prolonged apnea which causes activation of the vagal reflex. It should be noted that the recurrence of AF after electrical conversion was significantly higher in untreated patients compared to those treated with CPAP.

Chronic renal failure

Excessive daytime sleepiness is reported by most patients with end-stage renal disease; in these patients there are both central and obstructive respiratory components, leading to a prevalence of 40% -60% of SAS. Among the speculated mechanisms involved there is chronic hypoxia which can cause tubular apoptosis or changes in the epithelial-mesenchymal transfers that will cause exacerbation of renal fibrosis.

Sleep related breathing disorders have been described almost 200 years ago, but the treatment options that have transformed the diagnosis and intervention into priority have developed in the last 20 years. In the latest guidelines of the American College of Physicians linked to SAS management in adults, they recommended that the initial treatment should be CPAP therapy.

There are some ways to prevent the occurrence or progression of sleep apnea. First, it is important to maintain a low body mass index, as obesity is a major contributor to SAS; also, it is recommended to avoid drugs and substances that relax the airways and cause snoring (sedatives or alcohol). It was observed that a lateral position of the body during sleep minimizes any breathing problems encountered.

The answer to why some individuals with SAS get to be hypertensive and others do not, can be found in the complex multifactorial nature of this pathology. SAS is, however, only one of the many risk factors of hypertension and some individuals have an increased risk of developing hypertension related sleep apnea, while others may be genetically protected from the adverse effects of SAS.